Bibliographic Details
| Title: |
Wnt/β-Catenin Signaling Mediated-UCH-L1 Expression in Podocytes of Diabetic Nephropathy. |
| Authors: |
Hongxia Zhang, Weili Luo, Yonghong Sun, Yanchun Qiao, Liying Zhang, Zhilian Zhao, Shijun Lv |
| Source: |
International Journal of Molecular Sciences; Sep2016, Vol. 17 Issue 9, p1404, 13p, 6 Diagrams, 1 Chart, 2 Graphs |
| Subject Terms: |
DIABETIC nephropathies, CATENIN genetics, UBIQUITIN carboxy-terminal hydrolase, NEPHRITIS, CELL communication, CELL migration, GENETICS, DISEASE risk factors |
| Abstract: |
Increasing studies identified podocyte injury as a key early risk factor resulting in diabetic nephropathy (DN). The ubiquitin carboxy-terminal hydrolase 1 (UCH-L1) participates in podocyte differentiation and injury, which is elevated in the podocytes of a variety of nephritis. Whether UCH-L1 expression is positively related to podocyte injury of DN remains unclear. In this study, elevated expression of UCH-L1 and its intrinsic mechanism in high glucose (HG)-stimulated murine podocytes were investigated using western blot and real-time quantitative PCR. Kidney biopsies of DN patients and health individuals were stained by immunofluorescence (IF) method. The morphological and functional changes of podocytes were tested by F-actin staining and cell migration assay. Results demonstrated that HG induced upregulation of UCH-L1 and activation of the Wnt/β-catenin signaling pathway in podocytes. However, blocking of the Wnt pathway by dickkopf related protein 1 (DKK1) eliminated the above changes. Furthermore, IF staining confirmed that, compared with healthy individuals, the expression of UCH-L1 and β-catenin were obviously increased in kidney biopsy of DN patients. Overexpression of UCH-L1 remodeled its actin cytoskeleton, increased its cell migration and impacted its important proteins. All the findings manifested that Wnt/β-catenin/UCH-L1 may be a new potential therapy method in the treatment of DN in future. [ABSTRACT FROM AUTHOR] |
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| Database: |
Complementary Index |
